Acute hypoxia releases dopamine from glomus cells without altering the norepinephrine stores in carotid body. A similar pattern of changes in catecholamine content is elicited by the injection of muscarinic receptor agonists. Methyl atropine prevents the release of dopamine elicited by methacholine and by acute hypoxia, suggesting that a cholinergic muscarinic receptor may mediate dopamine release. In contrast, long lasting hypoxia increases dopamine and norepinephrine content in carotid body. The increase of catecholamine content is hyperplasia of glomus cells. Carbohydrate-active steroids increase the catecholamine content in carotid body suggesting that these steroids may exert trophic functions during long-lasting hypoxia.